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Biomedical subjects

A Bernard

Publications and source records attributed to A Bernard.

At least 307 records · Page 17Linked to original sources
PubMed1993

Serum laminin, hydrocarbon exposure, and glomerular damage.

It has been postulated that occupational exposure to hydrocarbons may damage the kidney and lead to glomerulonephritis and chronic renal failure. As laminin is a ubiquitous basement membrane component that seems to play a central part in the structure and function of basement membranes and as the normal renal filtration process is highly dependent on an intact glomerular basement membrane, the serum laminin concentration was examined in a population of workers exposed to hydrocarbons. The hydrocarbon exposure was assessed by exposure surrogates (exposure duration and exposure score). An interaction between occupational exposure to hydrocarbons and hypertension increased the laminin concentration whereas the laminin concentration decreased in workers exposed for a long time probably because of a selection effect. In a subgroup of printers exposed to toluene whose hippuric acid excretion had been recorded for several years this interaction was confirmed when the hippuric acid excretion was substituted for the other exposure indices. In the exposed group, the age-related decline in creatinine clearance was accelerated. These results seem to confirm that occupational exposure to hydrocarbons is a non-specific factor that may promote a deterioration of renal function.

Adult↗
PubMed1993

Once-a-day administration of amikacin in neonates: assessment of nephrotoxicity and ototoxicity.

Neonates, especially preterms, are known to have low glomerular filtration rates (GFR). This may result in elevated trough concentrations during multiple administration of aminoglycosides (AGs), potentially leading to nephro- and ototoxic reactions. The once-daily administration (q.d.) of AGs has been shown to be equally or better tolerated in adults and children than the conventional schedules (twice daily, b.i.d.; thrice daily, t.i.d.), while offering potential pharmacodynamic and nursing advantages. No data, however, are available for neonates. As a consequence, this pilot study was conducted in order to assess the tolerance of the once-a-day administration of amikacin in comparison with the twice daily dose regimen, in relation to the pharmacokinetics of the drug under these two schedules. 22 Male neonates (gestational age > or = 34 weeks; postnatal age < or = 2 days) were randomized to receive amikacin (AK) (15 mg/kg/day) q.d. (n = 10) or b.i.d. (n = 12) together with ampicillin (50 mg/kg/12 h). AK plasma levels were measured at days 1, 3, 5 and 7 of treatment just before the next dose (trough level) and 1 h after completion of infusion (peak level) and after 3 and 6 h only at day 1. Due to the small size of the samples, no difference in efficacy could be assessed and was not the aim per se. Glomerular dysfunction was assessed by creatinine clearance, and tubular injuries by the urinary excretion of proteins (retinol binding protein, beta 2-microglobulin, clara cell protein (P1) and microalbumin), enzymes (N-acetyl-beta-D-glucosaminidase, alkaline phosphatase, alanine aminopeptidase, and gamma-glutamyltransferase), and total phospholipids (TPL) in urine. Ototoxicity was assessed by brainstem auditory evoked potentials (BAEPs) at days 0, 3 and 9 of therapy. Eight healthy neonates served as controls. All patients showed a normal and similar increase of GFR during the first postnatal days. Proteinuria did not increase, but enzymuria and TPL increased significantly during the treatment in both AK groups without significant difference between groups. BAEPs at day 9 were not significantly different between treated and untreated patients. We conclude from this pilot study that, in the absence of more toxicity, the q.d. administration of AK in neonates of > or = 34 weeks of gestational age may be recommended over its bid schedule in view of its potential advantages.

Amikacin↗
PubMed1993

Biomonitoring exposure to metal compounds with carcinogenic properties.

Several metals such as arsenic, beryllium, chromium and nickel are carcinogenic to man when they occur in certain well-defined physicochemical forms. The carcinogenic potential of these metals is linked to their mutagenic properties. The determination of the metal or possibly of its metabolites in biological media and the cytogenetic examination of somatic cells are two methods that can currently be used to monitor exposure of populations at risk. Due to the use of inappropriate methodology, the value of the positive cytogenetic results published so far appears questionable. By contrast, the concentrations of metals in blood, urine, or other biological materials can be determined with accurate and precise methods. Although it does not permit a direct assessment of the carcinogenic risk, this approach is currently the most suitable for monitoring exposed populations.

Arsenic↗
PubMed1993

[Spontaneous pneumothorax. A comparison of thoracoscopy and thoracotomy].

The aims of this study were to assess the advantages of surgical thoracoscopy versus thoracotomy. Two 16-patient groups (thoracotomy, thoracoscopy) were compared. They were equivalent with regards to technique, age, etiology and lung dystrophy. Patients were called by phone to evaluate the surgical and functional results. The questionnaire was filled out by an independent physician who ignored the surgical technique used. Hospital stay was 7 +/- 2 days for thoracoscopy versus 11.5 +/- 5 days for thoracotomy (p < 0.003). During the J30 to J60 period of time, pain was mild in 94% of thoracoscopy cases and severe or unbearable in 69% of thoracotomy cases (p < 0.002). Mobility of the shoulder was fully recovered in all thoracoscopy patients within the first month versus only 62% of recovery at 3 months in the thoracotomy group (p < 0.0001). Working was possible at 1 +/- 0.8 month in the thoracoscopy group versus 2.6 +/- 0.8 months in the thoracotomy group (p < 0.002). Leisure activities were resumed at 2 +/- 1 month in the thoracoscopy group versus 4 +/- 1 months in the thoracotomy group (p < 0.0005). Only one relapse occurred in the thoracoscopy group. Thoracoscopy prevents the drawbacks of thoracotomy but keeps the same efficiency in the treatment of pneumothorax.

Adult↗
PubMed1992

Incorporation of [35S]sulfate into glomerular membranes of rats chronically exposed to cadmium and its relation with urinary glycosaminoglycans and proteinuria.

The aim of the present work was to assess the effects of long-term exposure to Cd on the sulfatation of glomerular membranes and their relation with proteinuria and urinary glycosaminoglycans (GAG). For this purpose the in vitro incorporation of [35S]sulfate was investigated in female Sprague-Dawley rats given 100 ppm of Cd in drinking water for 7 months. When compared with their controls, glomeruli from Cd-treated rats showed a 12.8% decrease in the incorporation of the label into glomerular membranes. This effect, which was not explained by differences in viability or in sulfate uptake by the glomeruli, suggests that sulfatation of glomerular membranes is impaired in Cd-treated rats. In support of this, in another independent experiment, a decrease, 17.4% on average, of the sulfate content of glomerular membranes was observed in long-term Cd-treated rats (100 ppm in drinking water for 4 months). This effect was significantly correlated with albuminuria and transferrinuria but not with beta 2-microglobinuria, suggesting that a loss of heparan sulfate of the glomerular capillary wall could be involved in the Cd-induced glomerular proteinuria. On the other hand an enhanced urinary excretion of GAG, negatively correlated with the sulfate content of glomerular membranes, was also observed in Cd-treated rats. Moreover GAG excretion was associated with tubular and glomerular proteinuria, which suggests that GAG might be a useful marker of Cd-induced nephrotoxicity.

Animals↗
PubMed1992

Human urinary protein 1: evidence for identity with the Clara cell protein and occurrence in respiratory tract and urogenital secretions.

Protein 1 (P1), a low mol mass urinary protein of unknown function, has been purified, sequenced and quantified in human biological fluids. The molecular size, subunit composition and partial amino acid sequence of P1 are similar to those of the 10 kDa Clara cell protein (CC10), a lung secretory protein. P1 is found in high concentrations in sputum, bronchoalveolar lavages, urine and semen of healthy individuals and in urine of some pregnant women. Contrary to what is claimed, P1 or CC10 is not a specific and unique product of the lung, but like its homologue in rabbits (uteroglobulin) it is also present in urogenital secretions. P1 or CC10 may act as a natural immunosuppressor protecting the respiratory and urogenital tracts from unwanted inflammatory reactions.

Adolescent↗
PubMed1992

CD58 and CD59 molecules exhibit potentializing effects in T cell adhesion and activation.

We have generated stable Chinese hamster ovary (CHO) cell transfectants expressing either CD58 or CD59 or both molecules to compare their respective parts played in T cell adhesion and activation. Using a rosetting assay, we have shown the following: 1) The CD59 molecule was directly responsible for adhesive interaction between human T cells and CD59+ CHO transfectants. CD59-mediated adhesion induced 12 +/- 2% (mean +/- SEM, n = 25) of rosettes. 2) The CD58 molecule expressed on CD58+ CHO transfectants induced 29 +/- 6% (mean +/- SEM, n = 8) of rosettes. 3) Double transfected CD58+CD59+ CHO cells formed up to 80% of rosettes, largely exceeding the sum of rosettes formed by single transfectants, thus disclosing at least an additive and possibly a synergic action of both molecules in mediating adhesion to T cells. Culturing purified human T cells in the presence of fixed CHO transfectants and submitogenic doses of PHA + rIL-1 alpha showed that: 1) CD59+ CHO transfectants induced sevenfold T cell proliferation enhancement, demonstrating the direct involvement of the CD59 molecule in T cell activation; 2) CD58+ CHO transfectants induced 20-fold T cell proliferation increase; and 3) the enhancement induced by CD58+CD59+ CHO cells was more than 40-fold. These results suggest that CD58 and CD59 molecules present on the surface of accessory cells might exert synergic function in T cell adhesive interactions and in the stimulation of T cell activation.

Animals↗
PubMed1992

CD59 molecule: a second ligand for CD2 in T cell adhesion.

The T cell surface molecule CD2 forms, with its counter-receptor CD58 (LFA-3), a powerful adhesion/activation pathway. There is some evidence that CD2 might bind more than a single ligand. Chinese hamster ovary cells (CHO) expressing human CD59 after cDNA transfection (CD59+CHO) form rosettes with human T cells; these rosettes are inhibited in a dose-dependent fashion by the CD59 monoclonal antibody (mAb) H19 and by the CD2 mAb O275 known to block natural rosettes, but not by the CD2R mAb D66, a poor rosette blocker. CD2+CHO transfectants form rosettes with human erythrocytes; these rosettes are inhibited by the CD59 mAb H19 in addition to CD2 mAb O275 and CD58 mAb; murine thymoma cells expressing human CD2 form rosettes with CD59+CHO cells that again are blocked by CD59 H19 and by CD2 O275 mAb. In a marked contrast with H19, two others CD59 mAb, YTH 53.1 and MEM 43, which react with a different epitope on CD59, led to a 50%-70% increase of the number of cells forming rosettes. In addition to rosette experiments, the binding of 125I-labeled CD59 molecules to CD2+CHO cells was specifically inhibited by unlabeled CD59 molecule and CD2 mAb. Furthermore, the binding of CD59 molecules to resting T cells induced expression of CD2R epitopes. These results directly show that CD2 binds CD59 and that subtle molecular changes occur upon binding.

Animals↗
PubMed1992

Plasma membrane water permeabilities of human oocytes: the temperature dependence of water movement in individual cells.

Membrane water permeability values were measured in individual fresh human pre-ovulatory oocytes using real time microscopy in a microscope diffusion chamber. The cells were exposed to anisosmotic conditions, their volume responses measured, and from these data the Lp values were computed employing the Kedem-Katchalsky analyses of irreversible thermodynamics. Lp values were measured at four temperatures for each oocyte between 37 degrees C and 10 degrees C, and the temperature-related Arrhenius activation energy (Ea) calculated. It was apparent that individual oocytes exhibited a wide range of Lp values; at 37 degrees C Lp values ranged between 0.33 and 1.80 microns/atm/min. However, each oocyte exhibited the expected inverse linear correlation between Lp and temperature, with high linear correlations (R2 values between 0.73 and 0.96). A mean value for Ea of 8.61 +/- 5.11 Kcal/mol was computed. It is apparent that pre-ovulatory human oocytes express a range of biological diversity in terms of membrane water transport, and this fact needs to be considered when attempting to formulate cryopreservation protocols for storage of these oocytes.

Cell Membrane Permeability↗
PubMed1992

Assessment of thyroid, testes, kidney and autonomic nervous system function in lead-exposed workers.

The objective of the study was to assess whether moderate occupational exposure to lead may be associated with early changes in potential target organs (thyroid, testes, kidney, autonomic nervous system). Workers exposed to lead in a lead acid battery factory (n = 98; mean blood lead 51 micrograms/dl, range 40-75 micrograms/dl) and 85 control workers were examined. None of the indicators of kidney function (in urine: retinol-binding protein, beta 2-microglobulin, albumin, N-acetyl-beta-D-glucosaminidase; in serum: creatinine, beta 2-microglobulin), endocrine function (follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, thyroxine, triiodothyronine) and autonomic nervous system (R-R interval variations on the electrocardiogram) were correlated with lead exposure (blood lead or duration of exposure) or showed significantly different mean values between the exposed group and controls. These results and an assessment of the published data suggest that compliance with the Directive of the Council of the European Communities on lead exposure (health surveillance in workers whose lead in blood exceeds 40 micrograms/dl and removal from exposure when blood lead exceeds 70-80 micrograms/dl) would prevent the occurrence of significant biological changes in the majority of lead-exposed workers.

Adult↗
PubMed1992

Loss of glomerular polyanion correlated with albuminuria in experimental cadmium nephropathy.

The relationship between proteinuria and glomerular polyanion (GPA) charge has been studied in a model of experimental cadmium (Cd) nephropathy. Female Sprague-Dawley rats were administered Cd in drinking water for up to 18 months. From month 2, the animals showed an elevation of albuminuria preceding by about 6 months the rise of urinary beta 2-microglobulin and IgG. The nephrotoxic action of Cd was not readily detectable on the basis of the urinary output of beta-N-acetylglucosaminidase, alanine aminopeptidase and lactate dehydrogenase. These enzymes showed either little variation or were affected late in the intoxication process. Administration of Cd for 12 or 18 months did not impair the GFR. The glomerular origin of the albuminuria induced by Cd was demonstrated by estimating the glomerular filtration of rat or human (injected intravenously) albumin in rats whose tubular reabsorption had been blocked by a saturating dose of cytochrome C. The GPA charge was assessed by measuring the binding of the cationic dye, Alcian blue (AB), to membranes of isolated glomeruli. The sialic and sulfate content of these membranes was also determined. The Cd induced-albuminuria was negatively correlated (r = -0.73; n = 37) with the AB binding to glomerular membranes, their sialic acid content (r = -0.39) but not with their sulfate content (r = -0.15). A negative correlation (r = -0.62; n = 37) was also observed between the albuminuria and red blood cell membrane negative charges largely contributed by sialic acid. All these observations can be interpreted as the evidence that Cd enhances the glomerular filtration of proteins through a GPA depletion involving mainly sialic acid.

Albuminuria↗
PubMed1992

Measurements of the membrane water permeability (Lp) and its temperature dependence (activation energy) in human fresh and failed-to-fertilize oocytes and mouse oocyte.

The volumetric response of oocytes during rapid alterations of the extracellular osmotic environment were recorded using video microscopy. From these observations, the kinetics of water loss for human and mouse oocytes were determined over the temperature range 37 to 10 degrees C, including 37, 30, 20, and 10 degrees C. The changes in diameter of oocytes were measured over a 5-min period and a computer model was used to derive values for membrane water permeability (Lp) and inactive volume (Vb) and to compare the experimental data to the predicted values. The results for the mouse oocyte Lp were comparable to values determined by other methods. However the human data, for both failed-to-fertilize and fresh oocytes, have a wide range of values with large standard deviations. The Lp values at the various temperatures were used to calculate the Arrhenius activation energy (Ea). An Ea value of 9.48 kcal/mol was found for the fresh mouse oocyte, whereas the activation energy for human oocytes was extremely low, 3.73 kcal/mol for fresh oocytes and 1.93 kcal/mol for failed-to-fertilize oocytes.

Animals↗
PubMed1992

Human and experimental studies on renal eicosanoid response to long-term cadmium exposure.

In order to assess the effects of long-term exposure to cadmium (Cd) on the renal metabolism of eicosanoids, the urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), and thromboxane B2 (TXB2) was determined in 37 workers exposed to Cd and in female Sprague-Dawley rats given 100 ppm Cd in drinking water for 10 months. Urinary output of sodium and calcium was also determined. The Cd-exposed workers showed an increased urinary concentration of 6-keto-PGF1 alpha, PGE2, sodium, and calcium. The rise of 6-keto-PGF1 alpha was related to Cd levels in blood and weakly correlated with urinary sodium. Calcium in urine was not related to the concentration of the metal in blood and urine. A slight elevation in urinary TXB2 was also observed in workers with blood Cd higher than 5 micrograms/liter. After 10 months of exposure to Cd, female Sprague-Dawley rats presented an enhanced urinary excretion of albumin, transferrin, beta 2-microglobulin, sodium, and PGE2 in urine. The latter was significantly correlated with albuminuria and transferrinuria. In conclusion the results show that chronic exposure to Cd induces changes in the urinary excretion of some eicosanoids. The possible relation of these changes to Cd-induced kidney dysfunction are discussed.

6-Ketoprostaglandin F1 alpha↗